Vestibular dysfunction due to ototoxic hair cell injury is a common cause of significant disability due to disequilibrium and inability to stabilize gaze during head movements. Although some patients with bilateral vestibular dysfunction are able to compensate through physical rehabilitation and reliance on other senses, those who fail to compensate currently have no good therapeutic options. Because the vestibular nerve should be intact in these patients, selectively applied electrical currents should be able to drive the nerve and elicit eye movements that can stabilize gaze. [unreadable] The central goal of this project is to further development toward an implantable neuroelectronic prosthesis capable of restoring vestibular function to people with symptomatic bilateral vestibular dysfunction. Although vestibular prosthesis development has lagged that of cochlear implants, one group has recently described a first prototype vestibular prosthesis. However, the eye movements it evoked were insufficient to stabilize gaze during natural head movements, and the experiments were performed on animals with normal vestibular function. It is unclear whether their results generalize to the case of a labyrinth damaged by ototoxicity or Meniere's disease. [unreadable] The proposed project will establish a physiologic and morphologic basis for vestibular prosthesis development, by refining a mammalian model of vestibular ototoxicity and by testing the biologic premises upon which prosthesis design is based. Because viable vestibular nerve afferents must exist for a prosthesis to stimulate, we will determine the effects of gentamicin toxicity on morphology and physiology of afferent fibers in semicircular canal crista. We will characterize the vestibulo-ocular reflex before and after bilateral treatment with ototoxic doses of intratympanic gentamicin. We will characterize the eye movements of bilaterally vestibular-deficient animals in response to single- and multi-canal patterned electrical stimulation of the semicircular canal cristae. We will test whether stimulation of canals in a single labyrinth can be combined to drive eye movements that cover the normal physiologic range. [unreadable] [unreadable]